Abhijeet Thakur, PhD
(He/Him/His)
Rank
Fellow or Postdoc
Department
Pediatrics
Newborn Medicine
Authors
Abhijeet Thakur, PhD*, Sule Cataltepe, MD
Principal Investigator
Sule Cataltepe
Twitter / Website
Categories
Bronchopulmonary dysplasia (BPD), a common complication of prematurity, is characterized by impaired alveolar development, likely driven by disrupted pulmonary vascularization. Recent single-cell transcriptomic analyses have identified two distinct capillary endothelial cell (EC) subpopulations in the lung: general capillary ECs (gCap/Cap1) and lung-specific aerocytes (aCap/Cap2). This study aimed to investigate the fate of these EC subpopulations in a mouse model of neonatal hyperoxia-induced lung injury, as well as in a state-of-the-art non-human primate (NHP) model of BPD. Specific markers for aCap (CA4, HPGD) and gCap (GPIHBP1) were used to assess the abundance and proliferative capacity of these EC subpopulations. We found a reduced abundance of both gCap and aCap in neonatal mouse lungs exposed to 7 days of hyperoxia (P1-P7) and in NHP BPD lungs compared to controls. Furthermore, we detected an increased proliferation index in gCap and a decreased proliferation index in aCap in both BPD models. In summary, our findings demonstrate that BPD is associated with a reduced abundance of both aCap and gCap populations. The relative increase in proliferating gCap cells in BPD suggests they may function as progenitors in vascular remodeling during neonatal lung injury.